Upregulated miR-146b-3p predicted rheumatoid arthritis development and regulated TNF-α-induced excessive proliferation, motility, and inflammation in MH7A cells.

IF 2.9 4区 医学 Q3 IMMUNOLOGY BMC Immunology Pub Date : 2024-06-20 DOI:10.1186/s12865-024-00629-9
Linxiao Ma, Huijie Liu, Ping Shao, Qian Lv
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Abstract

Background: Rheumatoid arthritis (RA) is a chronic immune system disease with a high disability rate threatening the living quality of patients. Identifying potential biomarkers for RA is of necessity to improve the prevention and management of RA.

Objectives: This study focused on miR-146b-3p evaluating its clinical significance and revealing the underlying regulatory mechanisms.

Materials and methods: A total of 107 RA patients were enrolled, and both serum and synovial tissues were collected. Another 78 osteoarthritis patients (OA, providing synovial tissues), and 72 healthy individuals (providing serum samples) were enrolled as the control group. The expression of miR-146b-3p was analyzed by PCR and analyzed with ROC and Pearson correlation analyses evaluating its significance in diagnosis and development prediction of RA patients. In vitro, MH7A cells were treated with TNF-α. The regulation of cell proliferation, motility, and inflammation by miR-146b-3p was assessed by CCK8, Transwell, and ELISA assays.

Results: Significant upregulation of miR-146b-3p was observed in serum and synovial tissues of RA patients, which distinguished RA patients and were positively correlated with the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-cyclic citrullinated peptide antibodies (anti-CCP), and rheumatoid factor (RF) of RA patients. TNF-α promoted the proliferation and motility of MH7A cells and induced significant inflammation in cells. Silencing miR-146b-3p alleviated the effect of TNF-α and negatively regulated the expression of HMGCR. The knockdown of HMGCR reversed the protective effect of miR-146b-3p silencing on TNF-α-stimulated MH7A cells.

Conclusions: Increased miR-146b-3p served as a biomarker for the diagnosis and severity of RA. Silencing miR-146b-3p could suppress TNF-α-induced excessive proliferation, motility, and inflammation via regulating HMGCR in MH7A cells.

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miR-146b-3p的上调预示着类风湿性关节炎的发展,并调控TNF-α诱导的MH7A细胞过度增殖、运动和炎症。
背景:类风湿关节炎(RA)是一种慢性免疫系统疾病,其高致残率威胁着患者的生活质量。确定 RA 的潜在生物标志物对于改善 RA 的预防和管理非常必要:本研究重点关注 miR-146b-3p,评估其临床意义并揭示其潜在调控机制:共纳入 107 例 RA 患者,采集血清和滑膜组织。材料:共收集了 107 名 RA 患者的血清和滑膜组织,另外 78 名骨关节炎患者(OA,提供滑膜组织)和 72 名健康人(提供血清样本)作为对照组。通过 PCR 分析 miR-146b-3p 的表达,并用 ROC 和 Pearson 相关性分析评估其在 RA 患者诊断和发展预测中的意义。在体外,用 TNF-α 处理 MH7A 细胞。通过CCK8、Transwell和ELISA试验评估了miR-146b-3p对细胞增殖、运动和炎症的调控作用:结果:在 RA 患者的血清和滑膜组织中观察到 miR-146b-3p 的显著上调,这与 RA 患者的红细胞沉降率(ESR)、C 反应蛋白(CRP)、抗环瓜氨酸肽抗体(anti-CCP)和类风湿因子(RF)呈正相关。TNF-α 促进了 MH7A 细胞的增殖和运动,并诱发了细胞的明显炎症。沉默miR-146b-3p可减轻TNF-α的影响,并负向调节HMGCR的表达。HMGCR的敲除逆转了沉默miR-146b-3p对TNF-α刺激的MH7A细胞的保护作用:结论:miR-146b-3p的增加可作为诊断RA及其严重程度的生物标志物。沉默miR-146b-3p可通过调节HMGCR抑制TNF-α诱导的MH7A细胞过度增殖、运动和炎症。
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来源期刊
BMC Immunology
BMC Immunology 医学-免疫学
CiteScore
5.50
自引率
0.00%
发文量
54
审稿时长
1 months
期刊介绍: BMC Immunology is an open access journal publishing original peer-reviewed research articles in molecular, cellular, tissue-level, organismal, functional, and developmental aspects of the immune system as well as clinical studies and animal models of human diseases.
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